New Hope for Sleep Apnea Patients May Be Coming

Sleep apnea induces acidosis, hypoxia, hypercarbia and increased blood pressure, which trigger an increase in cardiac ANS activity. Increased cardiac ANS activity leads to hemodynamic and electrophysiological shifts which actuate AF susceptibility. Studies that recorded intrinsic and extrinsic cardiac ANS activity in response to sleep apnea have demonstrated a mechanistic association between the cardiac ANS and sleep apnea-induced AF. Cardiac ANS is thought to mediate the electrophysiological responses of the atrial myocardium to apnea and thus, the cardiac afferents are a potential therapeutic target. According to Valderrábano, “Sleep apnea is highly associated with atrial fibrillation. The cardiac autonomic nervous system plays an important role in this association, and studies have shown that different components of this system could potentially be therapeutically targeted to decrease atrial fibrillation inducibility in patients with obstructive sleep apnea. Cardiac afferents are a crucial component of the cardiac autonomic nervous system and have therapeutic potential in reducing atrial fibrillation in those with sleep apnea.”Sleep apnea is a risk factor for the initiation, maintenance and recurrence of AF – although other risk factors such as age (over 60 years), presence of heart disease, hypertension and obesity also exist. Currently, treatments geared towards reducing the incidence or recurrence of AF mainly involve treatments that target sleep apnea. For instance, continuous positive airway pressure treatments improve patient-reported symptoms of sleep apnea such as snoring, daytime fatigue, restlessness during sleep and frequent nighttime awakenings. But these treatments also improve vascular parameters, AF symptoms and cardiovascular measures such as blood pressure. The intersection of sleep apnea and AF and how the cardiac ANS is mechanistically related to this nexus is critical to understand in order to develop better strategies for therapeutic interventions. Further studies and randomized clinical trials need to be conducted to discern if other components of the cardiac ANS, such as parasympathetic nerves, sympathetic nerves, epicardial ganglionated plexi or sensory afferents can be targeted for more effective management of AF in patients with sleep apnea. Collaborations between cardiologists, sleep medicine experts and clinical trial communities are imperative towards this end.